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作 者:刘术娟[1] 邱近明[1] 孙保存[1] 赵秀兰[1]
出 处:《中国动脉硬化杂志》1997年第2期121-125,共5页Chinese Journal of Arteriosclerosis
摘 要:为研究低密度脂蛋白经细胞修饰后对细胞受体的影响及前列腺素E2的作用,利用免疫细胞化学和生物亲和素-酶联免疫吸附法分别检测小鼠腹腔巨噬细胞清道夫受体、小鼠皮肤纤维母细胞低密度脂蛋白受体的结合活性,结果发现修饰组的巨噬细胞胞浆及胞膜有强阳性黄褐色颗粒,而药物组仅中度着色;修饰组低密度脂蛋白与其受体结合量(54±13μg/g细胞蛋白)较对照组(144±μg/g细胞蛋白)显著下降(P<0.01);药物组受体结合量(100±11μg/g细胞蛋白)较修饰组明显提高(P<0.05)。表明细胞修饰低密度脂蛋白能够刺激清道夫受体活性,抑制低密度脂蛋白受体活性;前列腺素E2(20mg/L)可对抗细胞修饰低密度脂蛋白对此二种受体的作用。Aim To investigate the influence of cell-modifiedlow density lipoprotein(cm-LDL) on scavenger recep-tors and low density lipoprotein receptors (LDLR ),meanwhile the effect of prostaglandin E2 (PGE2) wasstudied.Methods The receptor activity was detected bymeans of immunocytochemistry and bitin avidin-en-zyme linked immunosorbent assay(BA-ELISA), usingcultured murine peritoneal macrophages and murineskin fibroblasts as models.Results 1. The scavenger receptor activity onmacrophages increased in cm-LDL group, showingheavy brown granules in the membrane and cytoplasmof enlarged cells, while in PGE2 group, most cellswere mildly stained and in control group stained weak-ly. 2. The binding amount of LDL to LDLR on fi-broblasts showed that it markedly decreased in cm-LDL group (54±13 μg/g cell protein ) compared withwhich in control group (144± 8μg/g cell protein), P<0. 01 ; and significantly enhanced in PGE, group (100± 11μg/g cell protein), versus which in cm-LDLgroup, P<0. 05..Conclusion The findings suggested that cm-LDLstimulated scavenger receptor and inhibited LDLR,PGE2 (20 mg/L) markedly inhibited scavenger recep-tor activity and protected the LDLR against the injuryof oxidized LDL.
分 类 号:R543.502[医药卫生—心血管疾病] R977.6[医药卫生—内科学]
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